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Dissociation-related behaviors in mice emerge from the inhibition of retrosplenial cortex parvalbumin interneurons.

Yue Hu, Yifan Feng, Huoqing Luo, Xiao-Na Zhu, Siyu Chen, Kexin Yang, Ziqing Deng, Mengqiang Luo, Wenjie Du, Qi Wang, Shubai Wang, Kai Wei, Ji Hu, Yingwei Wang

Cell Reports January 28, 2025 DOI: 10.1016/j.celrep.2024.115086 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Mice
Interventions Ketamine optogenetic inhibition of RSC PV-INs
Topics Ketamine
Keywords Cp: neuroscience Dissociation Parvalbumin interneurons Phase-amplitude coupling Retrosplenial cortex Dissociative disorders Brain research Psychopharmacology Mental health
Citations 6
Key findings Ketamine inhibits retrosplenial cortex parvalbumin interneurons, enhancing delta oscillations and delta-gamma phase-amplitude coupling, which drives dissociation-like behaviors in mice; NR1 and HCN1 in these neurons are identified as ketamine targets that may cooperatively affect dissociation.

Abstract

Dissociation, characterized by altered consciousness and perception, underlies multiple mental disorders, but the specific neuronal subtypes involved remain elusive. In mice, we find that dissociation-inducing doses of ketamine significantly inhibit retrosplenial cortex (RSC) parvalbumin interneurons (PV-INs), enhancing delta oscillations (1-3 Hz) and delta-gamma phase-amplitude coupling (δ-γ PAC) and inducing dissociation-like behaviors. Optogenetic inhibition of RSC PV-INs triggers delta oscillations, δ-γ PAC, and some dissociation-like behaviors without ketamine. Furthermore, activation of RSC PV-INs or knockdown of the N-methyl-D-aspartate receptor subunit NR1 and the hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1) in RSC PV-INs attenuates ketamine-induced delta oscillations, δ-γ PAC, and certain dissociation-like behaviors. These findings reveal that PV-INs regulate delta oscillations and δ-γ PAC and identify NR1 and HCN1 as ketamine targets in PV-INs that may cooperatively affect dissociation, possibly providing potential therapeutic targets for dissociative symptoms.

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